目的探讨过氧化物酶6(peroxiredoxin-6,Prdx6)在弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)中的表达及其预后意义。方法回顾性分析286例DLBCL中Prdx6的表达及与临床病理特征和预后之间的关系。结果Prdx6在DLBCL中的表达...目的探讨过氧化物酶6(peroxiredoxin-6,Prdx6)在弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)中的表达及其预后意义。方法回顾性分析286例DLBCL中Prdx6的表达及与临床病理特征和预后之间的关系。结果Prdx6在DLBCL中的表达高于正常淋巴结(χ^(2)=17.69,P<0.001);Prdx6在non-GCB组中的表达高于GCB组(χ^(2)=21.771,P<0.001);Prdx6在有B症状病例的阳性表达强度高于无B症状病例(χ^(2)=4.872,P=0.027);Prdx6在乳酸脱氢酶(lactate dehydrogenase,LDH)升高病例中的阳性表达强度高于LDH正常病例(χ^(2)=5.965,P=0.015)。随访124例患者中,Prdx6强阳性组患者的预后比阴性组预后差(χ^(2)=6.998,P=0.008)。结论Prdx6在DLBCL中的表达较正常淋巴结高,且与non-GCB组、B症状和LDH有关。同时,Prdx6高表达与患者预后密切相关,提示可能对DLBCL的形成以及发生、发展机制具有一定作用。展开更多
Chinese forest musk deer(FMD),an endangered species,have exhibited low reproductive rates even in captivity due to stress conditions.Investigation revealed the presence of di(2-ethylhexyl)phthalate(DEHP),an environmen...Chinese forest musk deer(FMD),an endangered species,have exhibited low reproductive rates even in captivity due to stress conditions.Investigation revealed the presence of di(2-ethylhexyl)phthalate(DEHP),an environmental endocrine disruptor,in the serum and skin of captive FMDs.Feeding FMDs with maslinic acid(MA)has been observed to alleviate the stress response and improve reproductive rates,although the precise molecular mechanisms remain unclear.Therefore,this study aims to investigate the molecular mechanisms underlying the alleviation of DEHP-induced oxidative stress and cell apoptosis in primary peritubular myoid cells(PMCs)through MA intake.Primary PMCs were isolated and exposed to DEHP in vitro.The results demonstrated that DEHP significantly suppressed antioxidant levels and promoted cell apoptosis in primary PMCs.Moreover,interfering with the expression of PRDX6 was found to induce excessive reactive oxygen species(ROS)production and cell apoptosis in primary PMCs.Supplementation with MA significantly upregulated the expression of PRDX6,thereby attenuating DEHP-induced oxidative stress and cell apoptosis in primary PMCs.These findings provide a theoretical foundation for mitigating stress levels and enhancing reproductive capacity of in captive FMDs.展开更多
Peroxiredoxin-6(PRDX6)is an antioxidant enzyme with both the activities of peroxidase and phospholipase A2(PLA2),which is involved in regulation of many cellular reactions.However,the function of PRDX6 during virus in...Peroxiredoxin-6(PRDX6)is an antioxidant enzyme with both the activities of peroxidase and phospholipase A2(PLA2),which is involved in regulation of many cellular reactions.However,the function of PRDX6 during virus infection remains unknown.In this study,we found that the abundance of PRDX6 protein was dramatically decreased in foot-and-mouth disease virus(FMDV)infected cells.Overexpression of PRDX6 inhibited FMDV replication.In contrast,knockdown of PRDX6 expression promoted FMDV replication,suggesting an antiviral role of PRDX6.To explore whether the activity of peroxidase and PLA2 was associated with PRDX6-mediated antiviral function,a specific inhibitor of PLA2(MJ33)and a specific inhibitor of peroxidase activity(mercaptosuccinate)were used to treat the cells before FMDV infection.The results showed that incubation of MJ33 but not mercaptosuccinate promoted FMDV replication.Meanwhile,overexpression of PRDX6 slightly enhanced type I interferon signaling.We further determined that the viral 3Cprowas responsible for degradation of PRDX6,and 3Cpro-induced reduction of PRDX6 was independent of the proteasome,lysosome,and caspase pathways.The protease activity of 3Cprowas required for induction of PRDX6 reduction.Besides,PRDX6 suppressed the replication of another porcine picornavirus Senecavirus A(SVA),and the 3Cproof SVA induced the reduction of PRDX6 through its proteolytic activity as well.Together,our results suggested that PRDX6 plays an important antiviral role during porcine picornavirus infection,and the viral 3Cproinduces the degradation of PRDX6 to overcome PRDX6-mediated antiviral function.展开更多
Correction to:Virologica Sinica(2021)36:948-957 https://doi.org/10.1007/s12250-021-00352-4 Due to our negligence,the original version of this article,published online on March 15,2021,contained a mistake in Figure 2E(...Correction to:Virologica Sinica(2021)36:948-957 https://doi.org/10.1007/s12250-021-00352-4 Due to our negligence,the original version of this article,published online on March 15,2021,contained a mistake in Figure 2E(The Knockdown band of Western blotting was provided incorrectly).The correct Fig.2E is given below.We apologize for this error and state that this does not change the scientific conclusions of the article in any way.展开更多
文摘目的探讨过氧化物酶6(peroxiredoxin-6,Prdx6)在弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)中的表达及其预后意义。方法回顾性分析286例DLBCL中Prdx6的表达及与临床病理特征和预后之间的关系。结果Prdx6在DLBCL中的表达高于正常淋巴结(χ^(2)=17.69,P<0.001);Prdx6在non-GCB组中的表达高于GCB组(χ^(2)=21.771,P<0.001);Prdx6在有B症状病例的阳性表达强度高于无B症状病例(χ^(2)=4.872,P=0.027);Prdx6在乳酸脱氢酶(lactate dehydrogenase,LDH)升高病例中的阳性表达强度高于LDH正常病例(χ^(2)=5.965,P=0.015)。随访124例患者中,Prdx6强阳性组患者的预后比阴性组预后差(χ^(2)=6.998,P=0.008)。结论Prdx6在DLBCL中的表达较正常淋巴结高,且与non-GCB组、B症状和LDH有关。同时,Prdx6高表达与患者预后密切相关,提示可能对DLBCL的形成以及发生、发展机制具有一定作用。
基金supported by the Fund of Sci-Tech Innovation Program of Shaanxi Academy of Forestry(No.SXLK2021-0219)the Science and Technology Project of Shaanxi Province(No.2022SF-512)the Science and Technology Innovation and Achievement Transformation Project of Experimental Demonstration Station(base)of Northwest A&F University(No.TGZX2021-32)。
文摘Chinese forest musk deer(FMD),an endangered species,have exhibited low reproductive rates even in captivity due to stress conditions.Investigation revealed the presence of di(2-ethylhexyl)phthalate(DEHP),an environmental endocrine disruptor,in the serum and skin of captive FMDs.Feeding FMDs with maslinic acid(MA)has been observed to alleviate the stress response and improve reproductive rates,although the precise molecular mechanisms remain unclear.Therefore,this study aims to investigate the molecular mechanisms underlying the alleviation of DEHP-induced oxidative stress and cell apoptosis in primary peritubular myoid cells(PMCs)through MA intake.Primary PMCs were isolated and exposed to DEHP in vitro.The results demonstrated that DEHP significantly suppressed antioxidant levels and promoted cell apoptosis in primary PMCs.Moreover,interfering with the expression of PRDX6 was found to induce excessive reactive oxygen species(ROS)production and cell apoptosis in primary PMCs.Supplementation with MA significantly upregulated the expression of PRDX6,thereby attenuating DEHP-induced oxidative stress and cell apoptosis in primary PMCs.These findings provide a theoretical foundation for mitigating stress levels and enhancing reproductive capacity of in captive FMDs.
基金supported by grants from the National Key R&D Program of China(2017YFD0501103)the Key Development and Research Foundation of Yunnan(2018BB004)+1 种基金the Chinese Academy of Agricultural Science and Technology Innovation Project(Y2017JC55)Central Public-interest Scientific Institution Basal Research Fund(1610312016013 and 1610312017003)。
文摘Peroxiredoxin-6(PRDX6)is an antioxidant enzyme with both the activities of peroxidase and phospholipase A2(PLA2),which is involved in regulation of many cellular reactions.However,the function of PRDX6 during virus infection remains unknown.In this study,we found that the abundance of PRDX6 protein was dramatically decreased in foot-and-mouth disease virus(FMDV)infected cells.Overexpression of PRDX6 inhibited FMDV replication.In contrast,knockdown of PRDX6 expression promoted FMDV replication,suggesting an antiviral role of PRDX6.To explore whether the activity of peroxidase and PLA2 was associated with PRDX6-mediated antiviral function,a specific inhibitor of PLA2(MJ33)and a specific inhibitor of peroxidase activity(mercaptosuccinate)were used to treat the cells before FMDV infection.The results showed that incubation of MJ33 but not mercaptosuccinate promoted FMDV replication.Meanwhile,overexpression of PRDX6 slightly enhanced type I interferon signaling.We further determined that the viral 3Cprowas responsible for degradation of PRDX6,and 3Cpro-induced reduction of PRDX6 was independent of the proteasome,lysosome,and caspase pathways.The protease activity of 3Cprowas required for induction of PRDX6 reduction.Besides,PRDX6 suppressed the replication of another porcine picornavirus Senecavirus A(SVA),and the 3Cproof SVA induced the reduction of PRDX6 through its proteolytic activity as well.Together,our results suggested that PRDX6 plays an important antiviral role during porcine picornavirus infection,and the viral 3Cproinduces the degradation of PRDX6 to overcome PRDX6-mediated antiviral function.
文摘Correction to:Virologica Sinica(2021)36:948-957 https://doi.org/10.1007/s12250-021-00352-4 Due to our negligence,the original version of this article,published online on March 15,2021,contained a mistake in Figure 2E(The Knockdown band of Western blotting was provided incorrectly).The correct Fig.2E is given below.We apologize for this error and state that this does not change the scientific conclusions of the article in any way.